Acute Bone Pain following Renal Transplantation: Differentiation between Benign Bone Edema and Avascular Necrosis

Pilmore, Helen; Walker, Robert; McMillan, Bruce; Paranjpe, Dhananjay; Berkeley, Barrie

doi:10.1159/000013305

Cited by 8 publications

(5 citation statements)

References 11 publications

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“…It has been suggested that this disorder is a part of a spectrum of disorders affecting bone that includes reflex sympathetic dystrophy and transient osteoporosis. A number of previous studies have documented similar bone marrow edema patterns in the femoral head (14,15). Jagose et al (14) reported eight cases, including four who had knee involvement.…”

Section: Discussionmentioning

confidence: 80%

Transient Bone Marrow Edema in Renal Transplantation: A Distinct Post‐transplantation Syndrome with a Characteristic MRI Appearance

Coates

Tie

Russ

et al. 2002

American Journal of Transplantation

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We describe four patients who developed severe knee pain within 3 months of renal transplantation. Plain radiographs were normal and inflammatory markers (CRP, ESR) were all within normal ranges. Magnetic resonance imaging (MRI) showed a distinctive pattern in all four cases of bone marrow signal changes, extending from the epiphyseal region into the metaphyseal region in two cases. The appearances were different from those of avascular necrosis (AVN) and reflex sympathetic dystrophy and showed no progression to develop AVN during the follow-up period of 36 months. In all cases the pain resolved over a period of 3 months without specific therapy. Follow-up MRI scans were obtained in all patients after the pain had subsided, which revealed resolution of the MRI changes. We suggest that MRI be the investigation in such patients and that bone marrow edema changes will regress without the need to withdraw cyclosporin.

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Section: Discussionmentioning

confidence: 80%

Transient Bone Marrow Edema in Renal Transplantation: A Distinct Post‐transplantation Syndrome with a Characteristic MRI Appearance

Coates

Tie

Russ

et al. 2002

American Journal of Transplantation

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“…In 1998 Grandtnerova et al 12 and Pilmore et al, 13 described more cases of pain arising 2-3 months after renal transplant. In 1999 Torregrosa and Campistol 7 published a review on post-transplant RSDS in patients treated with cyclosporine, with a prevalence between 1 and 10%.…”

Section: Discussionmentioning

confidence: 99%

Calcineurin-inhibitor induced pain syndrome after organ transplantation

Collini

Bartolomeis

Barni

et al. 2006

Kidney International

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Among 243 patients who received kidney transplants at our center, two patients suddenly developed a severe debilitating pain syndrome in the lower limbs. Case no. 1A 49-year-old male patient who received a deceased donor kidney transplant, in therapy with tacrolimus (plus steroids and perioperative basiliximab). One month after transplantation he reported joint pain in his ankles, knees, feet, and hands. The pain became so intense that the patient was forced to use crutches to walk. Clinical examination revealed intense pain at movement, without edema, redness, increase in temperature, or cutaneous trophic alterations. The patient was receiving tacrolimus 5 mg b.i.d. with levels between 5 and 10 ng/ml. There was no clinical or serologic evidence of rheumatic disease or rhabdomyolysis. The rise in serum creatinine was attributed to heavy non-steroidal antiinflamatory drug use. After withdrawing these agents, the serum creatinine decreased to 1.6 mg/dl. Bone radiographies showed osteoporosis at the heads of the knee, ankle, tarsal, and metatarsal bones. An ultrasound scan of the joints highlighted a minimal amount of articular effusion and a mild synovial reaction in the knee and foot joints. Magnetic resonance imaging (MRI) of the left knee showed an area of bone marrow edema in the external condyle of the femur and wearing of the cartilage (Figure 1). Computerized bone mineralometry showed a slight reduction of the bone mass, whereas bone scintigraphy revealed increased radionuclide uptake in the affected joints (Figure 2).

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“…Osteonecrosis has been reported to develop following multiple episodes of CIPS, in which pain typical of CIPS responded initially to treatment with calcium channel blockers 15 . Also, symptoms of lower limb pain with MRI features of marrow oedema affecting the metatarsals, knees and hips have been reported to progress to osteonecrosis despite withdrawal of cyclosporine 17 …”

Section: Marrow Oedema and The Calcineurin‐induced Pain Syndromementioning

confidence: 99%

From marrow oedema to osteonecrosis: Common paths in the development of post‐transplant bone pain (Review Article)

Elder¹

2006

Nephrology

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Summary: Osteonecrosis, the calcineurin‐inhibitor‐induced pain syndrome and transient marrow oedema may occur after renal transplantation, are generally painful and can be diagnosed by X‐ray, radionuclide scan or magnetic resonance imaging. They share features of increased intraosseous pressure, compromised vascular supply, marrow oedema and the development of a ‘bone compartment syndrome’. Glucocorticoid dosage is the most commonly implicated risk factor for osteonecrosis. Mechanisms may include the differentiation of mesenchymal stem cells to adipocytes causing increased intraosseous pressure and collapse of marrow sinusoids, as well as increased osteoblast and osteocyte apoptosis. Some of these effects may be ameliorated by lipid lowering drugs. Calcineurin‐inhibitors, particularly cyclosporine, may increase the risk of osteonecrosis because of vasoconstrictive effects and sirolimus may influence the development of osteonecrosis by potentiating the effects of calcineurin inhibitors or by influencing the lipid profile. For osteonecrosis, early stages are generally managed conservatively or with core decompression sometimes accompanied by bone grafting and more recently the injection of bone morphogenic protein. The use of iloprost to improve blood flow and bisphosphonates and RANK‐ligand inhibition to reduce osteoclastic resorption of remaining trabecular structures are as yet unproven strategies. Unfortunately, the rate of total hip arthroplasty remains high. For the calcineurin‐inhibitor‐induced pain syndrome and transient marrow oedema, calcium channel blockers, the reduction or withdrawal of calcineurin‐inhibitors and core decompression have been used. Although a lack of randomized controlled trials makes management decisions difficult, early recognition of these bone pain syndromes affords the best opportunity for avoiding prolonged pain or joint replacement surgery.

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Acute Bone Pain following Renal Transplantation: Differentiation between Benign Bone Edema and Avascular Necrosis

Cited by 8 publications

References 11 publications

Transient Bone Marrow Edema in Renal Transplantation: A Distinct Post‐transplantation Syndrome with a Characteristic MRI Appearance

Transient Bone Marrow Edema in Renal Transplantation: A Distinct Post‐transplantation Syndrome with a Characteristic MRI Appearance

Calcineurin-inhibitor induced pain syndrome after organ transplantation

From marrow oedema to osteonecrosis: Common paths in the development of post‐transplant bone pain (Review Article)

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